Borowczak Jędrzej, Gąsiorek-Kwiatkowska Agnieszka, Szczerbowski Krzysztof, Maniewski Mateusz, Zdrenka Marek, Szadurska-Noga Marta, Gostomczyk Karol, Rutkiewicz Paula, Olejnik Katarzyna, Cnota Wojciech, Karpów-Greiner Magdalena, Knypiński Wojciech, Sekielska-Domanowska Marta, Ludwikowski Grzegorz, Dubiel Mariusz, Szylberg Łukasz, Bodnar Magdalena
Department of Tumor Pathology and Pathomorphology, Oncology Centre-Prof. Franciszek Łukaszczyk Memorial Hospital, 85-796 Bydgoszcz, Poland.
Department of Obstetrics, Gynaecology and Oncology, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, 85-168 Bydgoszcz, Poland.
Diseases. 2024 Jul 2;12(7):142. doi: 10.3390/diseases12070142.
SARS-CoV-2 can damage human placentas, leading to pregnancy complications, such as preeclampsia and premature birth. This study investigates the histopathological changes found in COVID-19-affected placentas.
This study included 23 placentas from patients with active COVID-19 during delivery and 22 samples from patients without COVID-19 infection in their medical history. The samples underwent histopathological examination for pathology, such as trophoblast necrosis, signs of vessel damage, or fetal vascular malperfusion.
Newborns from the research group have lower weights and Apgar scores than healthy newborns. In the COVID-19 group, calcifications and collapsed intervillous space were more frequent, and inflammation was more severe than in the healthy group. At the same time, the placenta of SARS-CoV-2-positive patients showed signs of accelerated vascular maturation. Trophoblast necrosis was found only in the placentas of the research group. The expression of CD68+ was elevated in the COVID-19 cohort, suggesting that macrophages constituted a significant part of the inflammatory infiltrate. The increase in lymphocyte B markers was associated with placental infarctions, while high levels of CD3+, specific for cytotoxic T lymphocytes, correlated with vascular injury.
SARS-CoV-2 is associated with pathological changes in the placenta, including trophoblast necrosis, calcification, and accelerated villous maturation. Those changes appear to be driven by T cells and macrophages, whose increased expression reflects ongoing histiocytic intervillositis in the placenta.
严重急性呼吸综合征冠状病毒2（SARS-CoV-2）可损害人类胎盘，导致妊娠并发症，如先兆子痫和早产。本研究调查了受新冠病毒病（COVID-19）影响的胎盘的组织病理学变化。
本研究纳入了23例分娩时患有活动性COVID-19患者的胎盘以及22例既往无COVID-19感染患者的样本。对样本进行组织病理学检查，以观察病理变化，如滋养层坏死、血管损伤迹象或胎儿血管灌注不良。
研究组新生儿的体重和阿氏评分低于健康新生儿。在COVID-19组中，钙化和绒毛间隙塌陷更为常见，炎症也比健康组更严重。同时，SARS-CoV-2阳性患者的胎盘显示出血管成熟加速的迹象。仅在研究组的胎盘中发现了滋养层坏死。COVID-19队列中CD68+的表达升高，表明巨噬细胞构成了炎症浸润的重要部分。淋巴细胞B标志物的增加与胎盘梗死有关，而细胞毒性T淋巴细胞特有的高水平CD3+与血管损伤相关。
SARS-CoV-2与胎盘的病理变化有关，包括滋养层坏死、钙化和绒毛成熟加速。这些变化似乎是由T细胞和巨噬细胞驱动的，它们表达的增加反映了胎盘持续存在的组织细胞绒毛间炎。
